Mirt2 alleviates LPS-induced inflammation of osteoblasts in alveolar bone destruction.

OBJECTIVES

The long noncoding RNA (lncRNA) myocardial infarction-associated transcript 2 (Mirt2) has been confirmed to affect several inflammatory diseases. This study was conducted to explore the functional mechanism of Mirt2 in inflammatory alveolar bone loss and its possibility of being a therapeutic target.

DESIGN

The expression level and potential role of Mirt2 in chronic inflammatory alveolar bone loss in mouse models of periodontitis and periapical periodontitis were investigated using micro-CT and qPCR. The characteristics of Mirt2 were evaluated by FISH, qPCR, ELISA, and alkaline phosphatase staining to confirm its function and mechanism of action in inflammatory response.

RESULTS

Mirt2 expression was significantly enriched in inflammatory alveolar bone diseases. Mirt2 expression increased upon LPS stimulation in MC3T3-E1 cells (P < 0.05), located at the cell cytoplasm. Mirt2 knockdown exacerbated the LPS-stimulated inflammatory response in MC3T3-E1 cells, whereas Mirt2 overexpression attenuated this effect and rescued LPS-impaired osteogenic differentiation.

CONCLUSIONS

lncRNA Mirt2 suggests a potential role in chronic inflammation-related bone loss, providing potential therapeutic target worthy of future investigation for inflammation-related bone loss.